姜黄素抑制由2,4,6-三硝基氯苯上调的表皮生长因子和双调蛋白，这与皮肤肿胀减轻相关。

Curcumin inhibits epigen and amphiregulin upregulated by 2,4,6-trinitrochlorobenzene associated with attenuation of skin swelling.

作者信息

Sakai Hiroyasu, Sato Ken, Sato Fumiaki, Kai Yuki, Mandokoro Kazutaka, Matsumoto Kenjiro, Kato Shinichi, Yumoto Tetsuro, Narita Minoru, Chiba Yoshihiko

机构信息

Division of Pharmacy Professional Development and Research, Department of Analytical Pathophysiology, School of Pharmacy, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.

Department of Pharmacology, School of Pharmacy, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.

出版信息

Inflamm Res. 2017 Aug;66(8):663-678. doi: 10.1007/s00011-017-1048-0. Epub 2017 Apr 12.

DOI:10.1007/s00011-017-1048-0

PMID:28405735

Abstract

OBJECTIVES

Contact dermatitis model involving repeated application of hapten is used as a tool to assess dermatitis, as characterized by thickening. Involvement of cell proliferation, elicited by repeated hapten-stimulation, in this swelling has been unclear. Curcumin is reported to reduce inflammation. We examined involvement of cell proliferation and the role of extracellular regulated kinase (ERK) in 2,4,6-trinitrochlorobenzene (TNCB) challenge-induced ear swelling. We also examined the effects of curcumin in this model.

METHODS

Mice were sensitized with TNCB to the abdominal skin. Then, they were challenged with TNCB to the ear three times. The ERK activation inhibitor U0126 or curcumin was applied 30 min before each TNCB challenge.

RESULTS

TNCB challenge-induced increased epidermal cell number and dermal thickening. Gene expressions of epithelial mitogen (EPGN), amphiregulin (AREG) and heparin-binding-epidermal growth factor (HB-EGF) were increased in the ears after the last TNCB challenge. Ki-67 immunoreactivity was increased in the dermis in TNCB-challenged ears. TNCB-induced swelling was inhibited by U0126 and curcumin. Curcumin also attenuated TNCB-induced ERK phosphorylation and expression of EPGN and AREG genes.

CONCLUSION

Ear swelling induced by TNCB challenge might be mediated, in part, by the EPGN- and AREG-ERK proliferation pathway and was inhibited by curcumin.

摘要

目的

涉及反复应用半抗原的接触性皮炎模型被用作评估以增厚为特征的皮炎的工具。反复半抗原刺激引发的细胞增殖在这种肿胀中的作用尚不清楚。据报道，姜黄素可减轻炎症。我们研究了细胞增殖的参与情况以及细胞外调节激酶（ERK）在2,4,6-三硝基氯苯（TNCB）激发诱导的耳部肿胀中的作用。我们还研究了姜黄素在该模型中的作用。

方法

用TNCB对小鼠腹部皮肤进行致敏。然后，对其耳部进行3次TNCB激发。在每次TNCB激发前30分钟应用ERK激活抑制剂U0126或姜黄素。

结果

TNCB激发诱导表皮细胞数量增加和真皮增厚。在最后一次TNCB激发后，耳部上皮有丝分裂原（EPGN）、双调蛋白（AREG）和肝素结合表皮生长因子（HB-EGF）的基因表达增加。在TNCB激发的耳部真皮中，Ki-67免疫反应性增加。U0126和姜黄素可抑制TNCB诱导的肿胀。姜黄素还可减弱TNCB诱导的ERK磷酸化以及EPGN和AREG基因的表达。